Fatty acid

Abstract: A photo-induced cyclic peroxidation in isolated chloroplasts is described In an osmotic buffered medium, chloroplasts upon illumination produce malondialdehyde (MDA)—a decomposition product of tri-unsaturated fatty acid hydroperoxides—bleach endogenous chlorophyll, and consume oxygen These processes show ( a ) no reaction in the absence of illumination; ( b ) an initial lag phase upon illumination of 10–20 minutes duration; ( c ) a linear phase in which the rate is proportional to the square root of the light intensity; ( d ) cessation of reaction occurring within 3 minutes after illumination ceases; and ( e ) a termination phase after several hours of illumination The kinetics of the above processes fit a cyclic peroxidation equation with velocity coefficients near those for chemical peroxidation The stoichiometry of MDA/O 2 = 002, and O 2 Chl bleached = 69 correlates well with MDA production efficiency in other biological systems and with the molar ratio of unsaturated fatty acids to chlorophyll The energies of activation for the lag and linear phases are 17 and 0 kcal/mole, respectively, the same as that for autoxidation During the linear phase of oxygen uptake the dependence upon temperature and O 2 concentration indicates that during the reaction, oxygen tension at the site of peroxidation is 100-fold lower than in the aqueous phase It is concluded that isolated chloroplasts upon illumination can undergo a cyclic peroxidation initiated by the light absorbed by chlorophyll Photoperoxidation results in a destruction of the chlorophyll and tri-unsaturated fatty acids of the chloroplast membranes

Abstract: Fatty acid methyl esters and dimethylacetals suitable for gas chromatographic analysis were prepared by treatment of lipids with boron fluoride–methanol (140 g BF3 per liter of methanol). This reagent is stable and easy to handle. Reaction conditions were investigated for triglycerides, diglycerides, monoglycerides, free fatty acids, sterol esters, phosphatidyl ethanolamines, phosphatidyl serines, phosphatidyl cholines, monophosphoinositides, monogalactosyl glycerides, phosphatidal cholines (choline plasmalogens), digalactosyl glycerides, and sphingomyelins. The methyl esters and dimethylacetals were readily purified by thin-layer chromatography, and yields were quantitative. There were few undesirable side reactions, and they did not affect the validity of the method. The procedure developed is simple, rapid, and generally applicable to lipids.

Abstract: fatty acids affect cardiac function (including antiarrhythmic effects), hemodynamics (cardiac mechanics), and arterial endothelial function have helped clarify potential mechanisms of action. The present Statement will address distinctions between plant-derived (-linolenic acid, C18:3n-3) and marine-derived (eicosapentaenoic acid, C20:5n-3 [EPA] and docosahexaenoic acid, C22:6n-3 [DHA]) omega-3 fatty acids. (Unless otherwise noted, the term omega-3 fatty acids will refer to the latter.) Evidence from epidemiological studies and RCTs will be reviewed, and recommendations reflecting the current state of knowledge will be made with regard to both fish consumption and omega-3 fatty acid (plant- and marine-derived) supplementation. This will be done in the context of recent guidance issued by the US Environmental Protection Agency and the Food and Drug Administration (FDA) about the presence of environmental contaminants in certain species of fish.

Abstract: Background: The effects of dietary fats on the risk of coronary artery disease (CAD) have traditionally been estimated from their effects on LDL cholesterol. Fats, however, also affect HDL cholesterol, and the ratio of total to HDL cholesterol is a more specific marker of CAD than is LDL cholesterol. Objective: The objective was to evaluate the effects of individual fatty acids on the ratis of total to HDL cholesterol and on serum lipoproteins. Design: We performed a meta-analysis of 60 selected trials and calculated the effects of the amount and type of fat on total:HDL cholesterol and on other lipids. Results: The ratio did not change if carbohydrates replaced saturated fatty acids, but it decreased if cis unsaturated fatty acids replaced saturated fatty acids. The effect on total:HDL cholesterol of replacing trans fatty acids with a mix of carbohydrates and cis unsaturated fatty acids was almost twice as large as that of replacing saturated fatty acids. Lauric acid greatly increased total cholesterol, but much of its effect was on HDL cholesterol. Consequently, oils rich in lauric acid decreased the ratio of total to HDL cholesterol. Myristic and palmitic acids had little effect on the ratio, and stearic acid reduced the ratio slightly. Replacing fats with carbohydrates increased fasting triacylglycerol concentrations. Conclusions: The effects of dietary fats on total:HDL cholesterol may differ markedly from their effects on LDL. The effects of fats on these risk markers should not in themselves be considered to reflect changes in risk but should be confirmed by prospective observational studies or clinical trials. By that standard, risk is reduced most effectively when trans fatty acids and saturated fatty acids are replaced with cis unsaturated fatty acids. The effects of carbohydrates and of lauric acid‐rich fats on CAD risk remain uncertain. Am J Clin Nutr 2003;77:1146‐55.